a) INHALATION: Remove patient to fresh air, and support patient with supplementary oxygen and ventilation as needed.
b) DERMAL: Immediately flush skin with large amounts of water and remove contaminated clothing as soon as possible.
c) OCULAR: Immediately flush eye(s) with water for at least 15 minutes.

a) Phenol and cresol have been found to induce glaucoma when injected into the eyes of rabbits and monkeys (Grant, 1993)

a) Hypotension that progressed to cardiovascular shock developed within one hour of injection of 30 mL of 89% phenol (26.9 g or 0.44 mg/kg of body weight) in a woman being treated for chronic pancreatitis pain (Christiansen & Klaman, 1996).
b) CASE REPORT: A 46-year-old woman developed unconsciousness, respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, leukocytosis, and severe metabolic acidosis after unintentional ingestion of 75 grams of resorcinol instead of glucose. Hypotension, acute lung injury, and oliguria occurred after she was transferred to an intensive care unit. Despite supportive therapy, she died several hours after ingestion (Bulut et al, 2006).
c) CASE REPORT: A 32-year-old man with nephrolithiasis developed hypotension (BP 70/40 mmHg) and tachycardia (85/min) after ingesting a spoonful of home-made extract of Juniperus oxycedrus containing phenol. After admission to the intensive care unit, his systolic blood pressure dropped to 40 mmHg despite intravenous fluid administration. Although he didn't experience chest pain, an ECG revealed sinus tachycardia with ST segment elevation in leads I, II, aVF, and V4, V5, V6 and ST segment depression in leads V1 and V2. In addition, elevated cardiac enzymes (CK 1,920 International Units/L, CK-MB 304 International Units/L, Troponin I 17.47 ng/mL) were observed. Echocardiography showed a left ventricular ejection fraction of 66%. Following supportive care, he recovered and was discharged home without further sequelae (Koruk et al, 2005).

a) Truppman and Ellenby (1979) reported dysrhythmias in 10 of 43 patients undergoing phenol chemical face peels. Dysrhythmias included premature ventricular contraction (4), bigeminy (2), paroxysmal atrial tachycardia (2), and ventricular tachycardia (2) (Truppman & Ellenby, 1979).
b) CASE REPORT: A 52-year-old woman developed hypotension and ventricular dysrhythmias following unintentional ingestion of 1 ounce of 89% phenol (Haddad et al, 1979).
c) CASE REPORT: Ventricular tachycardia developed 62 min after injection of 30 mL of a 89% phenol solution which contained approximately 26.9 g of phenol for a dose of 0.44 mg/kg of body weight (Christiansen & Klaman, 1996).
d) Atrial fibrillation and other dysrhythmias have occurred with chemical face peeling with phenol solutions (Gross, 1983) (Stuzin et al, 1983). Some patients had preexisting cardiac disease.
e) CASE REPORT: After undergoing mechanical dermabrasion and chemical peeling with phenol, an 11-year-old boy with xeroderma pigmentosum developed ventricular tachycardia with a pulse rate of up to 220 beats per minute. One day after the surgery, the urinary phenol concentration was 58.9 mg/dL (ref range 0-20.7 mg/dL). He recovered completely and was discharged home 7 days after surgery without further sequelae (Unlu et al, 2004).
f) Spontaneously-resolving premature ventricular contractions (PVCs) occurred during subtrigonal phenol injection therapy for severe urinary incontinence (Forrest & Ramage, 1987).

a) RATS: A study using laboratory rats, in which phenol was applied to the skin, found direct myocardial toxicity (decreased blood pressure and heart rate, S-T segment depression, and T-wave inversion). Death resulted from pulseless electrical activity (PEA) (Stagnone et al, 1987).

a) Because of its low volatility, phenol is not considered a serious respiratory risk through inhalation exposure (ACGIH, 2001; Hathaway et al, 1996). However, it can cause cardiorespiratory collapse through its systemic effects in acute poisoning (Raffle et al, 1994).

a) Tachypnea occurs after exposure (Pohanish, 2002).
b) CASE REPORT: A 32-year-old man with nephrolithiasis developed tachypnea (a respiratory rate of 22 beats/minute) and productive cough after ingesting a spoonful of home-made extract of Juniperus oxycedrus containing phenol. Following supportive care, he recovered and was discharged home without further sequelae (Koruk et al, 2005).

a) CASE REPORT: Following intercostal nerve block with phenol, a 51-year-old man developed a burning sensation in the pharynx, tachypnea, and bilateral inspiratory and expiratory wheezing and rhonchi, which was relieved by inhaled albuterol (Atkinson & Shupak, 1989).

a) SUMMARY: Adult respiratory distress syndrome and fatal respiratory failure have been reported following phenol poisoning (inhalation or ingestion) (Gupta et al, 2008; Dart et al, 2000; Fu et al, 2001).
b) Acute overexposure can result in noisy, difficult breathing, cough, rales, acute lung injury, and death due to respiratory failure (Budavari, 1996; ITI, 1995).
c) CASE REPORT: Marked hyperemia of the tracheal and bronchial mucous membranes and acute lung injury was seen on autopsy following an ingestion of 10-20g of phenol in a woman attempting suicide. She initially became comatose with partial absence of reflexes, skin pallor, increased respirations, weak and rapid pulse and nonreactive pupils. These symptoms progressed to cardiac and respiratory arrest and failed attempts to resuscitate (HSDB, 2003).
d) CASE REPORT: A 50-year-old man with chronic pain was inadvertently injected with 10 cc of 89% phenol (intended dose: 10 cc of 6% phenol) and developed immediate shortness of breath followed by hypoxia (ABG: pH 7.31; pCO2 14 mmHg; pO2 38 mmHg) requiring mechanical ventilation. Chest x-ray showed alveolar and interstitial opacities by day 2 of admission. Ventilatory support was continued for 4 days, with the patient successfully extubated. Clinical findings improved, but the patient continued to have persistent opacities on chest x-ray and multiple bilateral nodular opacities were observed on chest CT. At 6 months, lung nodules had resolved (Gupta et al, 2008).
e) CASE REPORT: A 39-year-old woman drank 600 mL of a chemical antiseptic which contained 15% ortho-phenylphenol in a suicide attempt. She developed progressive dyspnea and coma. On admission her pulse rate was 108 beats/minute and respiratory rate 34/minute. Chest x-ray showed increased alveolar infiltrates in bilateral upper lobes, especially the right upper lobe.
f) CASE REPORT: A 46-year-old woman developed unconsciousness, respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, leukocytosis, and severe metabolic acidosis after unintentional ingestion of 75 grams of resorcinol instead of glucose. Hypotension, acute lung injury, and oliguria occurred after she was transferred to an intensive care unit. Despite supportive therapy, she died several hours after ingestion. Autopsy results revealed acute lung injury, renal congestion, an eosinophilic substance in renal cortical tubular lumens, and hyperemia in all organs (Bulut et al, 2006).
g) CASE REPORT: Mild interstitial pulmonary edema in the left lung occurred in a 48-year-old man after experiencing dermal second-degree burns following contact with 15% phenol. His condition improved 3 days after intensive pulmonary care (Lin et al, 2006).

a) CASE REPORT: A 46-year-old woman developed unconsciousness, respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, leukocytosis, and severe metabolic acidosis after inadvertent ingestion of 75 grams of resorcinol instead of glucose. Despite supportive therapy, she died several hours after ingestion. Autopsy results revealed diffuse pulmonary edema, renal congestion, an eosinophilic substance in renal cortical tubular lumens, and hyperemia in all organs (Bulut et al, 2006).
b) Respiratory arrest occurred 30 minutes after ingestion of 26.7 g of phenol (Haddad et al, 1979).
c) CASE REPORT: Respiratory distress that resulted in intubation occurred approximately 30 minutes after injection of 30 mL of 89% phenol (26.9 g or 0.44 g/kg of body weight) in an adult (Christiansen & Klaman, 1996).
d) Respiratory failure may develop secondary to upper airway injury and/or CNS depression (Kamijo et al, 1999; Wu et al, 1998).

a) CASE REPORT: Acute epiglottitis resulting in life-threatening airway obstruction developed in a 49-year-old woman following use of a phenol-containing throat spray (Ho & Hollinrake, 1989).

a) Upper airway injury may result in stridor, as reported in 5% (4/72) of patients after ingestion of 26% phenol in a 5-year retrospective study (Spiller et al, 1993).

a) Phenol exposure results in headaches, dizziness, weakness, tremor, convulsions, unconsciousness, central nervous system depression and coma (ITI, 1995; Budavari, 1996).
b) CASE REPORT: A 32-year-old man with nephrolithiasis developed headache after ingesting a spoonful of home-made extract of Juniperus oxycedrus containing phenol (Koruk et al, 2005).

a) CASE REPORT: Seizures and death were reported following dermal exposure of less than 10% of the body surface area to a pure solution of 2,4-DICHLOROPHENOL in a 33-year-old man (Kintz et al, 1992).
b) CASE REPORT: A 52-year-old woman developed seizures following unintentional ingestion of 1 ounce of 89% phenol (Haddad et al, 1979).
c) CASE REPORT: A 7-year-old boy developed recurrent seizures 8 hours after sustaining dermal burns from cresol. Seizures recurred 4 days after exposure, but were controlled with benzodiazepines and valproate (Sakai et al, 1999).
d) CASE REPORT: A 46-year-old woman developed unconsciousness, respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, leukocytosis, and severe metabolic acidosis after unintentional ingestion of 75 grams of resorcinol instead of glucose. Despite supportive therapy, she died several hours after ingestion (Bulut et al, 2006).
e) CASE REPORT: A 27-year-old pregnant woman developed unconsciousness, drowsiness and tonic-clonic seizures following unintentional ingestion of 50 g of resorcinol. Following supportive therapy, she was discharged home on day 15. However, her newborn was pronounced dead approximately 24 hours after delivery (Duran et al, 2004).

a) Initially fleeting excitation may occur, but is quickly followed by seizures and unconsciousness (Kamijo et al, 1999; Sakai et al, 1999; Wu et al, 1998).
b) Spiller et al (1993) reported that 11% (9/72) of patients with acute oral exposures to a 26% phenol containing disinfectant experienced lethargy, while 2 developed coma. Onset of lethargy ranged from 15 minutes to 1 hour (Spiller et al, 1993).
c) CASE REPORT: An adult became comatose 4 hours after unintentional injection of 26.9 g of phenol (0.44 mg/kg of body weight) during therapy for chronic pain (Christiansen & Klaman, 1996).

a) FACIAL PALSIES/CASE REPORT: Repeated attacks of left-sided facial palsies occurred in a 42-year-old woman within minutes after exposure to increased air concentrations of chlorocresol (Dossing et al, 1986).

a) Extrapyramidal symptoms described as "neuroleptic-induced rabbit syndrome" were reported in a 65-year-old woman who ingested 70 mL of 42 to 52% phenol approximately 3 hours after presenting in a comatose state with flaccid extremities. It's suggested that phenol increased acetylcholine release with corresponding dopaminergic hypofunction, which resulted in perioral movements which were fine, rapid and rhythmic, along with Parkinsonian symptoms. No permanent sequelae were reported (Kamijo et al, 1999).

a) Phenol has been shown to be neurotoxic in animal studies. Mice exposed to varying phenol concentrations in drinking water were shown to have lower concentrations of neurotransmitters, including norepinephrine, dopamine, and 5-hydroxytryptamine (Hsieh et al, 1992).

a) ESOPHAGEAL BURNS: Ingestion of lethal amounts of produces severe burns of the mouth, pharynx, esophagus and gastrointestinal tract; perforation is possible (Hathaway et al, 1996; ITI, 1995). In one patient, endoscopy revealed diffuse esophageal ulcers compatible with grade IIb corrosive injury (Chen et al, 2005).
b) FINDINGS: White, necrotic lesions form in the mouth, esophagus and stomach (Budavari, 1996).
c) Of 17 patients who underwent endoscopy after ingesting a 26% phenol solution, 16 had first-degree burns and one had minor tissue sloughing (Spiller et al, 1993).

a) Nausea, vomiting, diarrhea, severe abdominal pain and difficulty swallowing result from exposure (Hathaway et al, 1996; Budavari, 1996; ITI, 1995)
b) Chlorinated drinking water contaminated with phenols resulted in the production of phenol, monochlorophenols, dichlorophenols, and trichlorophenols which were associated with a significant increase in gastrointestinal illness in the exposed population (Jarvis et al, 1985).
c) Gastrointestinal symptoms such as diarrhea, mouth sores, burning of the mouth and dark urine were the primary symptoms that appeared after consuming drinking water contaminated with phenol. On a 6 month follow-up, no residual health effects were found in the individuals who consumed the contaminated water (Baxter et al, 2000).
d) CASE REPORT: A 32-year-old man with nephrolithiasis developed nausea and vomiting after ingesting a spoonful of home-made extract of Juniperus oxycedrus containing phenol. Examination of his mouth showed several gingival erosions. Following supportive care, he recovered and was discharged home without further sequelae (Koruk et al, 2005).

a) A 65-year-old woman developed erosive duodenogastritis after ingesting 70 mL of 42% to 52% phenol (Kamijo et al, 1999).

a) Liver damage can occur after phenol exposure (Hathaway et al, 1996), which can result in jaundice (ITI, 1995) and death (Lewis, 2000).
b) CASE REPORT: A 43-year-old man presented to the hospital with jaundice, mild right upper quadrant tenderness, hematuria, and backache 6 days after phenol injection (2 mL of 5% phenol) sclerotherapy for hemorrhoids. The laboratory results revealed elevated serum urea 25.7 mmol/L (normal 2.8-7.6), serum creatinine 171 mcmol/L (normal 70-133), bilirubin 110 mcmol/L (normal 3-17), alkaline phosphatase 301 International Units/L (normal 45-122), and alanine aminotransferase 64 Units/L (normal 10-44). In addition, his INR was 1.1, serum albumin was low at 31 g/L (normal 38-47), and C-reactive protein was elevated at 264 (normal less than 6). He was diagnosed with hepatotoxicity with associated transient renal failure. After supportive care, he recovered and was discharged home a week later. However, he still had abnormal liver function tests for the next 6 months (Suppiah & Perry, 2005).
c) CASE REPORT: A 32-year-old man with nephrolithiasis developed hepatotoxicity after ingesting a spoonful of home-made extract of Juniperus oxycedrus containing phenol. Laboratory results showed mildly elevated liver enzymes (ALT 49 International Units/L, AST 66 International Units/L, LDH 329 International Units/L) which returned to normal concentrations on the fourth day postingestion (Koruk et al, 2005).
d) CASE REPORT: A 39-year-old woman drank 600 mL of a chemical antiseptic which contained 15% ortho-phenylphenol in a suicide attempt. She developed progressive dyspnea and coma. On admission her pulse rate was 108 beats/minute and respiratory rate 34/minute with intermittent tachypnea. Chest x-ray showed increased alveolar infiltrates in bilateral upper lobes, especially the right upper lobe.

a) CASE REPORT: Following contact with 15% to 99% phenol, four men suffered dermal burns on 7% to 10% of their total body surface areas. In the first 3 to 5 post-burn days, an elevation of liver enzymes (AST and ALT) was observed (Lin et al, 2006).
b) CASE REPORT: Marked elevations in aminotransferase concentrations (AST 10,450 International Units/L, ALT 8,990 International Units/L, LDH 15,580 International Units/L, and CPK 170 International Units/L) were reported in an initially asymptomatic 26-year-old female 24 hours after intentional ingestion of approximately 70 mL of a 50% cresol solution (Hashimoto et al, 1998). Hepatic enzyme concentrations had returned to baseline within 3 months of exposure.
c) CASE REPORT: After undergoing mechanical dermabrasion and chemical peeling with phenol, an 11-year-old boy with xeroderma pigmentosum developed ventricular tachycardia with a pulse rate of up to 220 beats per minute. In addition, elevated liver enzymes (AST, 62 Units/L; ALT, 23 Units/L; LDH, 744 Units/L) were observed. He recovered completely and was discharged home 7 days after surgery without further sequelae (Unlu et al, 2004).

a) Fatal neonatal hyperbilirubinemia has been reported following inhalation of phenolic vapors in poorly ventilated nurseries in which phenol has been used to disinfect bassinets and mattresses (HSDB, 2003).
b) CASE REPORT: A 27-year-old woman at 30 weeks of pregnancy unintentionally ingested 50 g of resorcinol, and developed unconsciousness, drowsiness, tonic-clonic seizures, hypothermia (35.2 degrees C), and respiratory failure. The laboratory analysis revealed leukocytosis, high bilirubin concentrations (direct-reacting bilirubin, 4.5; total bilirubin, 8 as highest concentrations), severe metabolic acidosis, and green-colored urine. Her newborn was pronounced dead approximately 24 hours after delivery. Following supportive therapy, she was discharged home on day 15 (Duran et al, 2004).

a) F344 rats given mixtures of low concentrations of phenol along with arsenic, benzene, chloroform, chromium, lead and trichloroethylene, showed hepatic proliferation after treatments up to 1 month (Constan et al, 1995).

a) Phenol exposure can produce kidney damage, with oliguria or anuria as well as albumin, casts, and red and white blood cells in urine (ITI, 1995).
b) CASE REPORT: A 50-year-old man with chronic pain was inadvertently injected with 10 cc phenol 89% (intended dose: 10 cc of 6% phenol) and developed oliguria on day 2 of admission. Hemodialysis was started for phenol clearance, but serum creatinine increased to 8.0 mg/dL by day 8. The patient was continued on intermittent hemodialysis (a dialysate flow rate of 500 mL/min and blood flow rate of 35 mL/min). Hemodialysis was discontinued on day 12. Gradually, myoglobinuria and proteinuria slowly improved and resolved by day 14. After acute symptoms resolved, the patient developed polyuria for several months. Renal function returned to normal within 6 months (Gupta et al, 2008).
c) CASE REPORT: A 46-year-old woman developed unconsciousness, respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, leukocytosis, and severe metabolic acidosis after unintentional ingestion of 75 grams of resorcinol instead of glucose. Hypotension, acute lung injury and oliguria occurred after she was transferred to an intensive care unit. Despite supportive therapy, she died several hours after ingestion. Autopsy results revealed diffuse acute lung injury, renal congestion, an eosinophilic substance in renal cortical tubular lumens, and hyperemia in all organs (Bulut et al, 2006).
d) CASE REPORT: A 39-year-old woman drank 600 mL of a chemical antiseptic which contained 15% ortho-phenylphenol in a suicide attempt. She developed progressive dyspnea and coma. On admission her pulse rate was 108 beats/minute and respiratory rate 34/minute with intermittent tachypnea. Chest x-ray showed increased alveolar infiltrates in bilateral upper lobes, especially the right upper lobe.
e) CASE REPORT: After falling into a vat of solvent containing 40% phenol in dichloromethane, a 41-year-old man developed acute renal failure, with renal cortical necrosis followed by renal papillary damage. He sustained renal injury and surface burns even though he avoided ingestion and was decontaminated rapidly (Foxall et al, 1989).
f) CASE REPORT: Acute renal failure (BUN 40 mg/dL, peak creatinine 9.8 mg/dL), mild gastrointestinal corrosive injury, and pneumonia occurred following intentional ingestion of 150 grams cresol in a 44-year-old man (Wu et al, 1998). Despite multiple complications, the patient recovered without sequelae following hemodialysis and intensive supportive therapy.
g) CASE REPORT: A 43-year-old man presented to the hospital with jaundice, mild right upper quadrant tenderness, hematuria, and backache 6 days after phenol injection (2 mL of 5% phenol) sclerotherapy for hemorrhoids. The laboratory results revealed elevated serum urea 25.7 mmol/L (normal 2.8-7.6), serum creatinine 171 mcmol/L (normal 70-133), bilirubin 110 mcmol/L (normal 3-17), alkaline phosphatase 301 International Units/L (normal 45-122), and alanine aminotransferase 64 Units/L (normal 10-44). In addition, his INR was 1.1, serum albumin was low at 31 g/L (normal 38-47), and C-reactive protein was elevated at 264 (normal less than 6). He was diagnosed with hepatotoxicity with associated transient renal failure. After supportive care, he recovered and was discharged home a week later. However, he still had abnormal liver function tests for the next 6 months (Suppiah & Perry, 2005).
h) CASE REPORT: A 32-year-old man with nephrolithiasis developed acute renal failure after ingesting a spoonful of home-made extract of Juniperus oxycedrus containing phenol. The urine examination revealed gross hematuria, leukocytes 10(5)/mL, proteinuria (1,000 mg/dL), and glucosuria (100 mg/dL). Following supportive care, he recovered and was discharged home without further sequelae (Koruk et al, 2005).

a) The renal insufficiency after phenol exposure can result in bloody urine (Pohanish, 2002). Urine color may be dark green, brown or black (Goldfrank et al, 1998; (Hashimoto et al, 1998; Sakai et al, 1999). Dark urine (bilirubin-negative) has been a prominent feature of occupational exposure to vaporized phenol (Goldfrank et al, 1998).
b) CASE REPORT: A 26-year-old woman presented with dark green urine after ingesting a product containing 50% cresol (Hashimoto et al, 1998).
c) CASE REPORT: A 27-year-old woman at 30 weeks of pregnancy unintentionally ingested 50 g of resorcinol, and developed unconsciousness, drowsiness, tonic-clonic seizures, hypothermia (35.2 degrees C), and respiratory failure. The laboratory analysis revealed leukocytosis, high bilirubin concentrations, severe metabolic acidosis (pH, 6.85; pCO2, 24 mmHg; PO2, 56 mmHg; HCO3, 3 mmol/L; BE, -25 mmol/L), and green-colored urine. Her newborn was pronounced dead approximately 24 hours after delivery. Following supportive therapy, she was discharged home on day 15 (Duran et al, 2004).

a) CASE REPORT: A 52-year-old woman developed metabolic acidosis following unintentional ingestion of 1 ounce of 89% phenol. The patient had a mixed acid-base disturbance characterized by respiratory alkalosis and metabolic acidosis throughout the first 24 hours post ingestion. The widest ion gap was 17 mEq/L. The acidosis responded to bicarbonate and potassium replacement (Haddad et al, 1979).
b) CASE REPORT: A 26-year-old woman presented with mild metabolic acidosis (pH 7.38, PaCO2 31 mmHg, HCO3 18 mmol/L) after ingesting a product containing 50% cresol (Hashimoto et al, 1998).
c) CASE REPORT: A 44-year-old man intentionally ingested 150 grams cresol and developed a mixed metabolic acidosis and respiratory alkalosis along with acute renal failure. The patient recovered following intensive supportive care (Wu et al, 1998).
d) CASE REPORT: A 46-year-old woman developed unconsciousness, respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, leukocytosis, and severe metabolic acidosis (pH 7.021, pCO2 60.5 mm Hg, pO2 45.5 mm Hg, HCO3 15.3 mmol/L, base excess 16.2 mmol/L) after unintentional ingestion of 75 grams of resorcinol instead of glucose. Despite supportive therapy, she died several hours after ingestion (Bulut et al, 2006).
e) CASE REPORT: A 27-year-old woman at 30 weeks of pregnancy unintentional ingested 50 g of resorcinol, and developed unconsciousness, drowsiness, tonic-clonic seizures, hypothermia (35.2 degrees C), and respiratory failure. The laboratory analysis revealed leukocytosis, high bilirubin concentrations, severe metabolic acidosis (pH, 6.85; pCO2, 24 mmHg; PO2, 56 mmHg; HCO3, 3 mmol/L; BE, -25 mmol/L), and green-colored urine. Her newborn was pronounced dead approximately 24 hours after delivery. Following supportive therapy, she was discharged home on day 15 (Duran et al, 2004).

a) Methemoglobinemia may develop after exposure to phenol (ACGIH, 2001).
b) CASE REPORT: A 46-year-old woman developed unconsciousness, respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, leukocytosis, and severe metabolic acidosis after unintentional ingestion of 75 grams of resorcinol instead of glucose. Despite supportive therapy, she died several hours after ingestion. Methemoglobin concentration of 10% was found in the blood sample obtained at the autopsy (Bulut et al, 2006).

a) Deep venous thrombosis has developed following injections of diluted phenol solutions (2% to 7%) used to produce either chemical neurolysis or motor point blocks for control of muscle spasticity in handicapped patients (Macek, 1983).

a) CASE REPORT: A 26-year-old woman developed hepatic injury and coagulopathy (PT 17.3 seconds with a control of 10.8 seconds) after ingesting a product containing 50% cresol (Hashimoto et al, 1998).

a) Hemolytic anemia may occur after exposure to phenol (ACGIH, 2001; Duran et al, 2004).
b) CASE REPORT: Following intentional ingestion of 300 mL of a 50% cresol solution (150 g), a 44-year-old man had multiple organ system complications, which included hemolysis, acute renal failure, and pneumonia (Wu et al, 1998). Complete recovery occurred after intensive supportive therapy.

a) CASE REPORT: A 32-year-old man with nephrolithiasis developed thrombocytopenia (a nadir of 51,000/mm(3) 2 days postingestion) after ingesting a spoonful of home-made extract of Juniperus oxycedrus containing phenol. Following supportive care, he recovered and was discharged home without further sequelae (Koruk et al, 2005).

a) CASE REPORT: A 46-year-old woman developed unconsciousness (Glasgow Coma Scale reading, 3 points), respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, leukocytosis (white blood cells 42,900/mm(3)), and severe metabolic acidosis after unintentional ingestion of 75 grams of resorcinol instead of glucose. Despite supportive therapy, she died several hours after ingestion (Bulut et al, 2006).
b) CASE REPORT: A 27-year-old woman at 30 weeks of pregnancy unintentionally ingested 50 g of resorcinol, and developed unconsciousness, drowsiness, tonic-clonic seizures, hypothermia (35.2 degrees C), and respiratory failure. The laboratory analysis revealed leukocytosis (25,000/mm(3)), high bilirubin concentrations, severe metabolic acidosis, and green-colored urine. Her newborn was pronounced dead approximately 24 hours after delivery. Following supportive therapy, she was discharged home on day 15 (Duran et al, 2004).

a) CASE STUDY: A study of 52 male workers and 30 male controls who were occupationally exposed to phenol alone or in combination with other solvents was conducted at an oil refinery in Egypt. Twenty of the males were exposed to phenol alone and 32 were exposed to phenol and other solvents including benzene, toluene and methylethylketone. Workers exposed to phenol alone or with the solvents had significantly elevated serum amino transferases, longer clotting times and lower creatinine concentrations than the control group. Prothrombin times were significantly increased in the phenol and solvent group.

a) MICE - Phenol has been shown to decrease peripheral red blood cell counts and hematocrits in mice given drinking water with varying concentrations of phenol (Hsieh et al, 1992).

a) Systemic toxicity and poisoning usually occurs by skin absorption, the main route of entry for solid, liquid or vapor phenol; the result can be lethal (ACGIH, 2001; AAR, 1996).

a) Skin irritation and sensitization may occur from using phenol containing products and have been reported during occupational exposure (Mancuso et al, 1996). Contact with the skin for prolonged periods may result in denaturation and gangrene followed by necrosis (Fisher, 1980).
b) Allergic contact dermatitis may rarely occur following the use of resorcinol in topical agents for the treatment of eczema (Langeland & Braathen, 1987).

a) SUMMARY: Abnormal pigmentation commonly occurs following dermal contact with phenolic compounds (Saunders et al, 1988; Tanaka et al, 1998). Deposition of dark pigment in the skin can result from prolonged contact with a dilute phenol solution (Hathaway et al, 1996).
b) CASE REPORT: Postmortem exam of a 27-year-old man presumed to have ingested a phenol compound had notably large areas on the skin surface (upper and lower extremities) that were dark brown in color as well as the lips and oral mucous membranes (Tanaka et al, 1998). The walls of the gastrointestinal tract and lungs were also dark brown and inflamed upon examination. Urine that was found in the bladder was reddish yellow in color.

a) Concentrated phenol may cause second- and third-degree burns (Lin et al, 2006; Grant, 1993; Fu et al, 2001) because of its caustic and defatting properties (Harbison, 1998). Phenol has local anesthetic properties that may allow extensive damage to occur before pain is recognized. The affected area may become white and opaque or dull gray, followed by a grey-white sloughing, then necrosis; this may lead to black gangrene (Saydjari et al, 1986; Raffle et al, 1994).
b) CASE REPORTS
c) ADULT

a) Intense diaphoresis may occur soon after exposure (Pohanish, 2002).

a) One case of contact allergy to phenol has been reported as a result of a phenol-formaldehyde resin in a knee guard. Patch tests were negative to formaldehyde, but positive for phenol (Vincenzi et al, 1992).

a) CASE REPORT: A 32-year-old man with nephrolithiasis developed myalgia after ingesting a spoonful of home-made extract of Juniperus oxycedrus containing phenol (Koruk et al, 2005).

a) ANTITHYROID ACTIVITY: Resorcinol has been reported to be goitrogenic and antithyroid per in vitro and in vivo experimental animal studies (Gaitan et al, 1987) .

a) Phenol has been shown to suppress the stimulation of cultured splenic lymphocytes in studies with mice (Hsieh et al, 1992).

a) In one review, phenol was said to affect the human embryo or fetus (Kuntz, 1976). Generally, substances that can induce methemoglobinemia are of particular concern for the fetus. Fetal hemoglobin is oxidized to methemoglobin more readily than the adult form is, and the fetus has a relatively higher demand for oxygen than does the adult.

a) In a Swedish reproductive epidemiological study of occupational exposure to disinfectants that included phenol and other substances, there was no clear association with risk for birth defects (Hernberg, 1983).

a) In mice, post-implantation mortality, fetal death, fetotoxicity, as well as specific developmental abnormalities of the musculoskeletal and craniofacial system in the offspring were seen (RTECS, 2003).
b) Treatment of F-344 rats by gavage on days 6 to 19 of gestation caused resorption and kinked-tail malformation, but maternal toxicity was also present (Narotsky & Kavlock, 1995).

a) Phenol has generally not been teratogenic in experimental animals, except at very high doses that were also toxic to the mothers (p 92). When injected in pregnant rats at a dose of 200 mg/kg, it had no effect (Minor & Becker, 1971). When given orally to rats at a dose of 120 mg/kg/day, it increased resorptions and caused low fetal weight, but was not teratogenic (p 120).

a) In the female rat, fetotoxicity was observed via the intraperitoneal route as well as fetotoxicity and post-implantation mortality by the oral route (RTECS, 2003).
b) Rats given up to 120 mg/kg of phenol by gavage on days 6 to 15 of gestation showed dose-related signs of fetotoxicity (Hathaway et al, 1996).
c) Rats exposed to up to 1.3 ppm of phenol throughout pregnancy showed increased pre-implantation loss and early postnatal death in the offspring (Hathaway et al, 1996).
d) Mice given up to 280 mg/kg of phenol by gavage on days 6 to 15 of gestation showed dose-related signs of fetotoxicity (Hathaway et al, 1996).
e) Phenol disrupted the estrus cycles in rats inhaling concentrations of 0.5 or 5 mg/m(3) for 3 months (Kolesnikova, 1972) and also caused pre-implantation deaths and early postnatal deaths under the same conditions (pp 149-153).

a) In a study of benzene and benzene metabolites in cultured rat embryos, phenol alone was minimally embryotoxic. However, phenol + S9 microsomal fraction resulted in dysmorphic and embryotoxic effects at a 0.01 M concentration. Generation of hydroquinone and catechol by microsomal oxidation was demonstrated by HPLC (Chapman et al, 1994).

a) One study concluded that phenol altered the sex ratio in rats at a concentration of 30 mg/m(3) and also suggested that the same effect could occur in humans (Malysheva, 1976).

a) Women and men working with phenol-formaldehyde resins were reported to have urogenital diseases (Ishchenko & Pushkina, 1978). Impotence occurred following acute phenol poisoning in one man (O'Donaghue, 1985), which may have been due to a general CNS effect rather than to a specific effect on the sex organs.

a) Listed as: Phenol
b) Carcinogen Rating: 3

a) An association between occupational exposure of US men to chlorophenol and nasal and nasopharyngeal cancers was observed (Mirabelli et al, 2000). The duration of exposure seemed to be a positive correlation in both types of cancers. The intensity of exposure also seemed to be a risk factor for nasopharyngeal cancer.

a) A 50-year-old male railroad worker presented with an erythematous, tender skin lesion on the right knee. The lesion had been present and intermittently tender for several years. When it did not resolve, it was biopsied, revealing squamous cell carcinoma in situ. The patient had worked for the railroad for 30 years and was exposed to coal tar creosote-treated railroad ties and lumber almost daily. The ties and timber he carried, handled and kneeled on were heavily coated with creosote and the creosote commonly coated his work clothes at the end of his work shifts (Carlsten et al, 2005).

a) Free phenol: 0 to 4 mg/100 mL
b) Conjugated phenol: 0.1 to 2 mg/100 mL
c) Total phenol: 0.15 to 7.96 mg/100 mL

a) A pre-employment examination should be done. Liver function, kidney function, and urinary phenol should be examined and documented. Examinations should be repeated after exposure and compared with pre-employment concentrations (Pohanish, 2002; HSDB, 2003).

a) Persons with known hepatic or kidney diseases should not be exposed to phenol for any length of time. Even intermittent exposure to vapors, particularly when handled at elevated temperatures, may become dangerous (HSDB, 2003).

a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:

a) Treatment of seizures may include the use of diazepam or phenobarbital.
b) Treatment of methemoglobinemia may require the use of oxygen and methylene blue.

a) Decontamination of dermal exposures with polyethylene 300 or 400 or isopropyl alcohol may be considered.

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

a) Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.

a) INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules (Prod Info PROVAYBLUE(TM) intravenous injection, 2016) and 10 mg/1 mL (1% solution) vials (Prod Info methylene blue 1% intravenous injection, 2011). REPEAT DOSES: Additional doses may be required, especially for substances with prolonged absorption, slow elimination, or those that form metabolites that produce methemoglobin. NOTE: Large doses of methylene blue may cause methemoglobinemia or hemolysis (Howland, 2006). Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection (Prod Info methylene blue 1% intravenous injection, 2011; Herman et al, 1999). NEONATES: DOSE: 0.3 to 1 mg/kg (Hjelt et al, 1995).
b) CONTRAINDICATIONS: G-6-PD deficiency (methylene blue may cause hemolysis), known hypersensitivity to methylene blue, methemoglobin reductase deficiency (Shepherd & Keyes, 2004)
c) FAILURE: Failure of methylene blue therapy suggests: inadequate dose of methylene blue, inadequate decontamination, NADPH dependent methemoglobin reductase deficiency, hemoglobin M disease, sulfhemoglobinemia, or G-6-PD deficiency. Methylene blue is reduced by methemoglobin reductase and nicotinamide adenosine dinucleotide phosphate (NADPH) to leukomethylene blue. This in turn reduces methemoglobin. Red blood cells of patients with G-6-PD deficiency do not produce enough NADPH to convert methylene blue to leukomethylene blue (do Nascimento et al, 2008).
d) DRUG INTERACTION: Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome (U.S. Food and Drug Administration, 2011; Stanford et al, 2010; Prod Info methylene blue 1% IV injection, 2011).

a) DOSE: 2 to 4 mg/kg intravenously over 5 minutes. Dose may be repeated in 30 minutes (Nemec, 2011; Lindenmann et al, 2006; Kiese et al, 1972).
b) SIDE EFFECTS: Hypotension with rapid intravenous administration. Vomiting, diarrhea, excessive sweating, hypotension, dysrhythmias, hemolysis, agranulocytosis and acute renal insufficiency after overdose (Dunipace et al, 1992; Hix & Wilson, 1987; Winek et al, 1969; Teunis et al, 1970; Marquez & Todd, 1959).
c) CONTRAINDICATIONS: G-6-PD deficiency; may cause hemolysis.

a) Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalemia, hypocalcemia, and hypomagnesemia). Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion.

a) LIDOCAINE/INDICATIONS
b) LIDOCAINE/DOSE
c) LIDOCAINE/MAJOR ADVERSE REACTIONS
d) LIDOCAINE/MONITORING PARAMETERS

a) AMIODARONE/INDICATIONS
b) AMIODARONE/ADULT DOSE
c) AMIODARONE/PEDIATRIC DOSE
d) ADVERSE EFFECTS

a) PROCAINAMIDE/INDICATIONS
b) PROCAINAMIDE/ADULT LOADING DOSE
c) PROCAINAMIDE/CONTROLLED INFUSION
d) PROCAINAMIDE/ADULT MAINTENANCE DOSE
e) PROCAINAMIDE/PEDIATRIC LOADING DOSE
f) PROCAINAMIDE/PEDIATRIC MAINTENANCE DOSE
g) PROCAINAMIDE/PEDIATRIC MAXIMUM DOSE
h) MONITORING PARAMETERS
i) AVOID

a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.

a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).

a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
b) DOSE

a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984a; Gaudreault et al, 1983a; Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992)

a) Advancing across the cricopharynx under direct vision
b) Gently advancing with minimal air insufflation
c) Never retroverting or retroflexing the endoscope
d) Using a pediatric flexible endoscope
e) Using extreme caution in advancing beyond burn lesion areas
f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).

a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding, and perforation is related to the severity of the initial burn (Zargar et al, 1991):
b) Grade 0 - Normal examination
c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.

a) ANIMAL
b) HUMAN

a) STUDY - In a study of 11 children with deep circumferential esophageal burns after caustic ingestion, insertion of a silicone rubber nasogastric tube for 5 to 6 weeks without steroids or antibiotics was associated with stricture formation in only one case (Wijburg et al, 1989).

a) STUDY - In a retrospective study of patients with extensive transmural esophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (esophagoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) The authors noted that this form of long chain PEG solution may require further study, but noted the relatively easy access to Golytely(R) in most emergency centers.

a) CHLORASEPTIC(R) LOZENGES contain 32.5 milligrams of phenol per lozenge as well as menthol (10 milligrams/lozenge) and benzocaine (6 milligrams/lozenge).
b) The recommended dose for adults and children over 12 years old is 1 lozenge every 2 hours if needed.
c) A total daily dose of 390 milligrams of phenol is possible (Prod Info, 1991).
d) 0.6 to 1.3 grams daily has been used therapeutically in adults (Leider & Moser, 1961).
e) The higher dose has produced side effects of giddiness, weak pulse, and increased perspiration.

a) CHLORASEPTIC(R) LIQUID (includes spray, gargle, and aerosol spray) contains 1.4 percent phenol (Prod Info, 1991).
b) SPRAY(PUMP) - Available in 6 fluid ounce bottle containing a total of 2.52 grams of phenol and 12.5 percent ethanol.
c) GARGLE - Available in 12 fluid ounce bottle containing a total of 5.04 grams of phenol and 12.5 percent ethanol.
d) AEROSOL SPRAY - Available in 1.5 ounce nitrogen propelled aerosol spray bottle containing a total of 0.63 gram of phenol.

a) CHILDREN 2 TO 12 YEARS - Spray 3 times and swallow every 2 hours if needed.

a) CHILDREN 6 TO 12 YEARS - Gargle with 10 milliliters for 15 seconds and expectorate every 2 hours.

a) CHILDREN 2 TO 12 YEARS - Spray directly on affected area for 1 second and swallow every 2 hours.

a) DERMAL
b) ORAL

1) Phenol

a) TWA: 5 ppm (19 mg/m(3))
b) STEL:
c) Ceiling: 15.6 ppm (60 mg/m(3)) [15-minute]
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: [skin]
f) Note(s):

a) IDLH: 250 ppm
b) Note(s): Not Listed

a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

a) D : Not classifiable as to human carcinogenicity.

a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.

a) Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)

a) 8-hour TWA:

a) 180 mg/kg

a) 270 mg/kg

a) 344 mg/kg

a) 127 mg/kg

a) 317 mg/kg
b) 530 mg/kg
c) 414 mg/kg

a) 669 mg/kg

a) 650 mg/kg
b) 460 mg/kg

a) 100 mcg/m(3) for 24H/61D-C
b) 5 mg/m(3) for 4H/17W-I
c) 150 mcg/m(3) for 8H/26W-I

a) Signs include gastroenteritis, painful abdomen, weakness, depression, and sternal recumbency.

a) SUMMARY
b) CASE REPORTS

a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.

a) Oral exposure may result in the following:
b) SMALL ANIMALS
c) LARGE ANIMALS

a) Dermal exposure may result in the following:
b) A solvent cleaner with both hydrophilic and hydrophobic portions may be used to remove phenol from the skin surface if readily available prior to irrigation.
c) Undiluted polyethylene glycol 300 or 400 may be a useful solvent (Brown et al, 1975), however it was not shown to be more effective than copious (deluge) quantities of water in animals (Pullin et al, 1978).
d) The area should be repeatedly sponged with a number of sponges soaked in PEG. Decontamination personnel should wear rubber gloves. A soapy bath is taken after treatment.
e) Multiple daily applications of PEG for several days to full thickness on skin injuries in rabbits resulted in renal failure and increased osmolal gap (Herold et al, 1982). There are no data to suggest that a single exposure to PEG for treatment of a phenol burn would be harmful.
f) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

a) Wash skin, apply sodium bicarbonate (0.5%) dressings.

a) Give oral adsorbent. Fluid and electrolyte therapy.

a) N-acetylcysteine may prevent renal and hepatic damage.
b) DOSE - 140 mg/kg intravenously followed by 50 mg/kg every 4 hours for 15 doses (Coppock et al, 1988).

a) Methylene blue 8 mg/kg intravenously or ascorbic acid 50 mg/kg intravenously. Ascorbic acid is the drug of choice in cats (Coppock et al, 1988).

1) Begin treatment immediately.
2) Keep animal warm.
3) Sample vomitus, blood, urine, and feces for analysis.
4) If skin exposure has occurred, wash animal thoroughly with a mild detergent and flush with copious amounts of water.
5) ANIMAL POISON CONTROL CENTERS

1) ORAL EXPOSURE
2) DERMAL EXPOSURE